Brain Research最新文献

{"title":"Altered neurotransmitters in cerebrospinal fluid of children with autism spectrum disorder","authors":"Ziwen Shi ,&nbsp;Yulin Jin ,&nbsp;Haiping Xu ,&nbsp;Lin Gao ,&nbsp;Manhong Wu ,&nbsp;Yanqun Chang ,&nbsp;Xingrong Song ,&nbsp;Xinying Guo","doi":"10.1016/j.brainres.2025.149851","DOIUrl":"10.1016/j.brainres.2025.149851","url":null,"abstract":"<div><h3>Introduction</h3><div>Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder characterized by social deficits and repetitive behaviors. Neurotransmitter imbalances have been implicated in ASD, but few studies have examined cerebrospinal fluid (CSF) alterations in ASD patients. Identifying specific CSF biomarkers could enhance our understanding of the underlying neurobiology and improve diagnostic and therapeutic approaches.</div></div><div><h3>Methods</h3><div>CSF samples were collected from 17 children, including 8 with ASD and 9 typically developing controls. Liquid chromatography–tandem mass spectrometry (LC-MS/MS) was used to analyze neurotransmitter levels and metabolites in the CSF samples. Statistical comparisons were performed to identify group differences in neurotransmitter concentrations.</div></div><div><h3>Results</h3><div>ASD participants had significantly lower levels of glutamine, norepinephrine, and kynurenine compared to controls. Neurotransmitter dysregulation, particularly in the glutamine-glutamate cycle, was observed in ASD, potentially contributing to core symptoms.</div></div><div><h3>Conclusion</h3><div>Our findings suggest that neurotransmitter imbalances in the CSF could serve as potential biomarkers for ASD. Further research is needed to validate these findings and explore therapeutic interventions targeting these neurotransmitter pathways.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1865 ","pages":"Article 149851"},"PeriodicalIF":2.6,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144727765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prenatal famine exposure and late-life functional brain network connectivity: A longitudinal study","authors":"Amber Boots ,&nbsp;Jessica S. Damoiseaux ,&nbsp;Youjin Jung ,&nbsp;Aline Marileen Wiegersma ,&nbsp;Anouk Schrantee ,&nbsp;Daphne E. Boucherie ,&nbsp;Tessa J. Roseboom ,&nbsp;Susanne R. de Rooij","doi":"10.1016/j.brainres.2025.149859","DOIUrl":"10.1016/j.brainres.2025.149859","url":null,"abstract":"<div><div>The effects of the prenatal environment on resting-state functional connectivity in the brain can be detected up into older adulthood. We previously identified differences in resting-state functional connectivity of the default mode network (DMN), salience network (SN), and central executive network (CEN) at age 68 between men and women in the Dutch famine birth cohort who had been exposed or unexposed to famine in early gestation. Here, we investigated longitudinal changes in resting-state functional connectivity of the DMN, SN and CEN between ages 68 (n = 115) and 74 (n = 80) in the same cohort. Within- and between-network functional connectivity of the DMN, SN and CEN were compared between individuals unexposed (born before or conceived after) or exposed to famine in early gestation using a latent change score modeling approach with full information maximum likelihood estimation. No group differences were observed in baseline within-network functional connectivity (intercept; Δχ² = 1.41; p = 0.70) or rate of change (slope; Δχ² = 0.20; p = 0.98) of the DMN, SN and CEN between individuals exposed or unexposed to famine in early gestation. Given the poor fit of the between-network model including group status, differences between exposed and unexposed groups could not be explored. Across both groups, there was a significant increase in DMN connectivity over time and an increased negative functional connectivity between the DMN and SN. This study did not reveal more pronounced aging-related alterations in network connectivity among individuals exposed to famine in early gestation compared to unexposed individuals. Thereby, this study does not provide evidence for accelerated brain aging-related patterns of resting-state functional connectivity after prenatal famine exposure.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1865 ","pages":"Article 149859"},"PeriodicalIF":2.6,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144717481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Does parental diet alter the neurobehaviour and the reflex and somatic parameters of the offspring?","authors":"Rafael Oliveira Pinheiro ,&nbsp;Juliana Késsia Barbosa Soares ,&nbsp;Anne Caroline Alves Vieira ,&nbsp;Maria Luiza Rolim Bezerra ,&nbsp;Geyse Araújo Costa ,&nbsp;Mariany Bernardino da Silva Barbalho ,&nbsp;Artur D’ Angelo da Silva Andrade ,&nbsp;Angela Maria Tribuzy de Magalhães Cordeiro ,&nbsp;Adriano Francisco Alves ,&nbsp;Alana Natalícia Vasconcelos de Araújo ,&nbsp;Jailane de Souza Aquino","doi":"10.1016/j.brainres.2025.149860","DOIUrl":"10.1016/j.brainres.2025.149860","url":null,"abstract":"<div><h3>Background</h3><div>The early-life nutritional environment plays crucial role in shaping offspring development. While most studies have assessed maternal or paternal high-fat diet (HFD) exposure independently, the combined impact of both remains poorly understood across developmental, metabolic, and behavioural parameters. This study evaluated the effects of maternal and paternal HFD consumption on offspring metabolism, neurodevelopment, and anxiety-like behaviour.</div></div><div><h3>Methods</h3><div>Male and female Wistar rats were randomised into four dietary groups (n = 10/group): NF/NF (both sexes received a normal-fat diet, NFD), HF/NF (only males received an HFD), NF/HF (only females received an HFD), and HF/HF (both sexes received an HFD). Offspring were assessed for physical growth, somatic maturation, reflex ontogeny (postnatal days 0–21), anxiety-like behaviours (open field and elevated plus maze tests), lipid profile, brain fatty acid composition, and prefrontal cortex histology.</div></div><div><h3>Results</h3><div>NF/HF and HF/HF groups showed delayed somatic growth and altered physical development. Reflex maturation was impaired in HF/NF and NF/HF offspring. Anxiety-like behaviours were more evident in NF/HF and HF/HF groups. The HF/HF group exhibited elevated total cholesterol (439.28 ± 71.88 mg/dL), higher LDL (151.11 ± 28.72 mg/dL), reduced HDL (36.84 ± 18.93 mg/dL), reduced neuronal cell body size, and lower levels of brain polyunsaturated fatty acids.</div></div><div><h3>Conclusion</h3><div>Combined maternal and paternal HFD intake exerts cumulative adverse effects on offspring, impairing physical development, reflex maturation, behaviour, and brain lipid composition. These findings provide novel evidence that parental nutritional status prior to conception jointly influences offspring neurobiological and metabolic trajectories, underscoring the importance of considering both maternal and paternal diets in early-life health strategies.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1865 ","pages":"Article 149860"},"PeriodicalIF":2.6,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144717480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alzheimer’s disease: a jigsaw puzzle comprised of different types of programmed cell death pieces","authors":"Yu Wang ,&nbsp;Dan Mu ,&nbsp;Ying Li ,&nbsp;Chang Liu ,&nbsp;Jianan Feng ,&nbsp;Yong Lai ,&nbsp;Guanhua Lou","doi":"10.1016/j.brainres.2025.149861","DOIUrl":"10.1016/j.brainres.2025.149861","url":null,"abstract":"<div><div>Alzheimer’s disease (AD), a prevalent neurodegenerative disorder among elderly populations, arises from complex interactions between genetic and environmental risk factors. Currently affecting over 55 million elderly individuals globally, AD cases are projected to reach approximately 150 million by 2050 due to demographic aging trends. AD is characterized by extracellular accumulated amyloid plaques (Aβ plaques), intracellular aggregated neurofibrillary tangles (NFTs), and extensive neurodegeneration caused by neuronal and neural cell death. Many investigations have proven assorted types of programmed cell death (PCD) contribute to the neurodegenerative process of AD, and many review articles have summarized the role of PCD in AD pathogenesis. While numerous experimental studies have demonstrated the involvement of various programmed cell death (PCD) pathways in Alzheimer’s disease (AD) pathogenesis, existing review articles lack comprehensive mechanistic integration. This review systematically evaluates all PCD-AD associations, including apoptosis, autophagy, necroptosis, parthanatos, phagoptosis, pyroptosis, NETosis, ferroptosis, and cuproptosis. Different from other existing reviews, this paper emphasizes that the pathogenesis of AD results from the combined involvement of multiple types of PCD (programmed cell death), rather than isolated pathways. Additionally, the roles of valence-variable metal ions in the pathogenesis of AD are also discussed.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1865 ","pages":"Article 149861"},"PeriodicalIF":2.7,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144702393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Study on the role and mechanism of intermittent theta burst stimulation (iTBS) induced N-acetylaspartylglutamate (NAAG) in suppressing ferroptosis in ischemic stroke","authors":"Hanqing Zhao ,&nbsp;Yingli Bi ,&nbsp;Shiyan Wang ,&nbsp;Yuan Yin ,&nbsp;Linyan Huang ,&nbsp;Wan Wang ,&nbsp;Xiang Wang ,&nbsp;Suhua Qi ,&nbsp;Zunke Gong","doi":"10.1016/j.brainres.2025.149830","DOIUrl":"10.1016/j.brainres.2025.149830","url":null,"abstract":"<div><div>This study investigates the mechanism through which intermittent theta burst stimulation (iTBS) inhibits ferroptosis in ischemic stroke by inducing N-acetylaspartylglutamate (NAAG). In SD rats subjected to middle cerebral artery occlusion (MCAO), iTBS treatment significantly decreased ischemia–reperfusion (I/R) injury, improving motor, coordination, spatial memory abilities and Cognitive Impairment by enhancing synaptic function and neuronal repair. Western blot analysis showed that in MCAO rats treated with iTBS, GPX4 protein expression increased, while ACSL4, TFRC, and DMT1 protein levels decreased. Furthermore, malondialdehyde (MDA), a product of lipid peroxidation, was significantly reduced. The antioxidant levels of SOD and GSH were notably elevated, while the content of iron ions decreased. These results indicate that iTBS effectively inhibits ferroptosis by reducing oxidative stress and iron accumulation. Metabolomic analysis has revealed a novel finding that iTBS increases the levels of NAAG and inhibits its rate-limiting enzyme FOLH1 (GCP-II), thereby decreasing excitatory glutamate production, improving glutathione metabolism, and subsequently suppressing ferroptosis. In vitro experiments demonstrated that NAAG and 2-PMPA (a FOLH1 inhibitor) improved cell survival and antioxidant capacity in an oxygen-glucose deprivation/reperfusion (OGD/R) model, suppressing ferroptosis. In conclusion, iTBS exerts a neuroprotective effect by regulating the synthesis and metabolism of NAAG, enhancing antioxidant capacity and iron metabolism, and delaying ferroptosis. This research provides new insights into potential treatments for Post-Stroke Cognitive Impairment.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1865 ","pages":"Article 149830"},"PeriodicalIF":2.7,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144714405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Detection of PPID-interacting proteins in migraine rats by IP-MS and validation by bioinformatics analysis and experiments","authors":"Yicheng Wang ,&nbsp;Haonan Fu ,&nbsp;Yonglie Zhao","doi":"10.1016/j.brainres.2025.149854","DOIUrl":"10.1016/j.brainres.2025.149854","url":null,"abstract":"<div><h3>Objective</h3><div>This study was conducted to detect the trigeminal nucleus caudalis (TNC) site and Peptidyl-prolyl cis–trans isomerase D (PPID)-interacting proteins in migraine rats and further investigate the mechanisms involved in migraine attacks.</div></div><div><h3>Methods</h3><div>In this study, a two-time nitroglycerin (NTG) injection (NTG-2) group and a three-time NTG injection (NTG-3) group were established to observe the changes in behavior, mitochondria morphology, and PPID expression. Besides, the TNC samples of migraine rats were collected to analyze the proteins that can bind to PPID by immunoprecipitation combined with mass spectrometry (IP-MS). In addition, relevant pathways were analyzed by bioinformatics. Finally, the results were verified by protein docking and Co-immunoprecipitation (Co-IP) experiments.</div></div><div><h3>Results</h3><div>The results demonstrated that in the TNC site of migraine rats, PPID expression was up-regulated with an increase in the injection times of NTG. Through a literature retrieval, it was found that the proteins that bound to PPID and were related to migraine mainly comprised G-protein-coupled receptor kinase interacting proteins 2 (Git2), Talin 1 (Tln1), sodium/potassium-transporting ATPase subunit alpha-3 (Atp1a3), and proteinase-activated receptor 2 (F2rl1). The protein docking results all exhibited a good docking ability. The Co-IP experiment results revealed that PPID and Atp1a3 can bind to each other.</div></div><div><h3>Conclusion</h3><div>PPID can play a role in migraine attacks <em>via</em> the mitochondrial-inflammatory pathway by interacting with Git2, Tln1, Atp1a3, and F2rl1.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1865 ","pages":"Article 149854"},"PeriodicalIF":2.7,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144702486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beta-sitosterol mitigates type 2 diabetes-induced cognitive deficits: a behavioral and molecular investigation in Swiss albino mice","authors":"Priyanka Swarnkar ,&nbsp;Prabha Rajput","doi":"10.1016/j.brainres.2025.149858","DOIUrl":"10.1016/j.brainres.2025.149858","url":null,"abstract":"<div><div>This study examines the long-term effects of diabetes, focusing on its association with cognitive impairment, and investigates the neuroprotective potential of β-sitosterol (BST) against cognitive deficits induced by type 2 diabetes mellitus (T2DM). T2DM was induced in Swiss albino mice using a cafeteria (CAF) diet for four weeks followed by a single dose of streptozotocin (STZ) (45 mg/kg, i.p.). Weekly assessments of body weight and blood glucose levels were conducted, along with behavioral evaluations using the radial arm maze (RAM), nest building test, and novel object recognition test (NORT) to assess spatial learning and memory. Additionally, lipid profile (TC, TG, LDL, HDL), biochemical markers (GSH, CAT, MDA), molecular markers (IL-1β, TNF-α, IL-10, Akt, Gsk-3β), and histopathological analyses were performed. Treatment with β-sitosterol (10 mg/kg and 20 mg/kg, p.o.) and metformin (200 mg/kg, i.p.) significantly improved cognition, as observed in behavioral tasks, by restoring antioxidant levels, increasing the anti-inflammatory marker IL-10 and neuroprotective Akt, and reducing MDA, IL-1β, TNF-α, and Gsk-3β compared to the T2DM group. β-sitosterol also ameliorated glucose and lipid metabolism abnormalities in T2DM mice. These findings suggest that the cognitive benefits of β-sitosterol and its combination therapy may be attributed to its neuroprotective effects, which are likely mediated through its antioxidant and anti-inflammatory activities.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1865 ","pages":"Article 149858"},"PeriodicalIF":2.7,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144702391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Two-hit immune activation induced autism-like phenotypes in mice: The underlying mechanism may involve the lung–brain axis","authors":"Chunxia Li ,&nbsp;Zhengguang Geng ,&nbsp;Yang Liu ,&nbsp;Xiaoqin Li ,&nbsp;Tianqi Wang ,&nbsp;Mashaal Ahmad ,&nbsp;Heng Luo ,&nbsp;Hao Zhou ,&nbsp;Yuxia Cui","doi":"10.1016/j.brainres.2025.149850","DOIUrl":"10.1016/j.brainres.2025.149850","url":null,"abstract":"<div><div>Neuroinflammation plays important roles in the pathogenesis and development of autism spectrum disorder (ASD). However, the mechanism by which peripheral organ inflammation affects neuroinflammation is still unclear. This study aimed to investigate that the interaction between the lungs and the brain as a potential mechanism underlying this effect. Ovalbumin (OVA) can induce neuroinflammation and cause neurotoxicity, leading to tissue damage or cognitive memory impairment. OVA – induced maternal immune activation (MIA) provides a stable animal model for studying ASD and other human neurodevelopmental disorders. Postnatal reinfection is an additional risk factor for ASD and may lead to pathological and physiological changes. Here we compared the expression of cytokines in the hippocampus and lung tissues of MIA offspring after the second acute immune stimulation at three times post birth, as well as the correlation between cytokines and autism-like phenotypes.Interestingly, our research findings suggest that maternal and postpartum OVA-induced immune activation and lung injury may produce an autistic phenotype, with potential mechanisms involving the lung- brain axis.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1865 ","pages":"Article 149850"},"PeriodicalIF":2.7,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144702392","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: Chronic non-communicable diseases that affect the central nervous system can be prevented through developmental plasticity.","authors":"Ana Elisa Toscano, Cristiane Matté","doi":"10.1016/j.brainres.2025.149855","DOIUrl":"10.1016/j.brainres.2025.149855","url":null,"abstract":"","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":" ","pages":"149855"},"PeriodicalIF":2.7,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144706314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Social interactions between attachment partners increase inter-brain plasticity","authors":"Linoy Schwartz ,&nbsp;Jonathan Levy ,&nbsp;Carmel Salomonski ,&nbsp;Itai Peleg ,&nbsp;Olga Hayut ,&nbsp;Orna Zagoory ,&nbsp;Ruth Feldman","doi":"10.1016/j.brainres.2025.149856","DOIUrl":"10.1016/j.brainres.2025.149856","url":null,"abstract":"<div><div>Inter-brain synchrony between interacting partners is an important feature of social brain function, but whether neural coordination persists beyond the immediate social moment is unknown. Using hyperscanning EEG, we investigated whether a brief mother-adolescent face-to-face interaction induces sustained changes in inter-brain synchrony. We measured neural synchrony in the fronto-temporal network of 110 mothers and adolescents (55 dyads) during co-present resting-state recordings before and after a naturalistic, positively-valanced face-to-face interaction. We found enhanced inter-brain synchrony in the fronto-temporal network following the social interaction, indicating that positive social exchanges can temporarily modify patterns of neural synchrony. The magnitude of this post-interaction neural synchrony was mediated by the partners’ behavioral synchrony during the interaction. Oxytocin increase from pre- to post-interaction predicted the increase in neural synchrony above and beyond behavioral synchrony, suggesting a distinct neuroendocrine path for inter-brain coordination. Results indicate that positive social interactions between attachment partners can induce short-term changes in neural synchrony that persist beyond the immediate exchange. Our findings suggest a potential mechanism by which repeated social experiences within attachment relationships may influence neural development and highlight the need to consider inter-brain dynamics in research on the social foundations of brain development.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1865 ","pages":"Article 149856"},"PeriodicalIF":2.7,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144706233","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}